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Synergy between plasminogen activator inhibitor-1 and Snail in tumoral migration

ABSTRACT: Snail, a family of transcriptional repressors implicated in cell movement, has been correlated with tumour invasivity. The Plasminogen Activation system (PAs), including urokinase (uPA), its receptor (uPAR), and its inhibitor (PAI-1), also plays a key role in cancer invasion and metastasis, either through proteolytic degradation or by non proteolytic modulation of cell adhesion and migration. Thus, Snail and PAs both influence those processes and are over-expressed in cancers. In this study we aimed to determine first whether Snail activity is correlated with PAs components expression and second how this correlation can influence tumoral cell migration. Keywords: Tumoral migration Comparison the invasive breast cancer cell-line MDA-MB-231 expressing Snail (MDA-Neo) with its derived clone expressing a dominant negative form of Snail (Snail-DN). Expression of PAs mRNAs was performed by cDNA microarrays and real time quantitative RT-PCR. Wound healing assay was used to determine cell migration. PAI-1’s distribution was assessed by immunostaining.

ORGANISM(S): Homo sapiens

SUBMITTER: Fabre-Guillevin E

PROVIDER: S-ECPF-GEOD-10395 | biostudies-other | 2008

REPOSITORIES: biostudies-other

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Project description:Due to controversial evidence in the literature pertaining to the activity of plasminogen activator inhibitor-1 in platelets, we examined the effects of residual platelets present in plasma (a potential pre-analytical variable) on various plasminogen activator inhibitor-1 and plasminogen activator inhibitor-1-related assays. Blood samples were collected from 151 individuals and centrifuged at 352 and 1500 g to obtain plasma with varying numbers of platelet. In a follow-up study, blood samples were collected from an additional 23 individuals, from whom platelet-poor (2000 g), platelet-containing (352 g) and platelet-rich plasma (200 g) were prepared and analysed as fresh-frozen and after five defrost-refreeze cycles (to determine the contribution of in vitro platelet degradation). Plasminogen activator inhibitor-1 activity, plasminogen activator inhibitor-1 antigen, tissue plasminogen activator/plasminogen activator inhibitor-1 complex, plasma clot lysis time, β-thromboglobulin and plasma platelet count were analysed. Platelet α-granule release (plasma β-thromboglobulin) showed a significant association with plasminogen activator inhibitor-1 antigen levels but weak associations with plasminogen activator inhibitor-1 activity and a functional marker of fibrinolysis, clot lysis time. Upon dividing the study population into quartiles based on β-thromboglobulin levels, plasminogen activator inhibitor-1 antigen increased significantly across the quartiles while plasminogen activator inhibitor-1 activity and clot lysis time tended to increase in the 4th quartile only. In the follow-up study, plasma plasminogen activator inhibitor-1 antigen was also significantly influenced by platelet count in a concentration-dependent manner. Plasma plasminogen activator inhibitor-1 antigen levels increased further after complete platelet degradation. Residual platelets in plasma significantly influence plasma plasminogen activator inhibitor-1 antigen levels mainly through release of latent plasminogen activator inhibitor-1 with limited effects on plasminogen activator inhibitor-1 activity, tissue plasminogen activator/plasminogen activator inhibitor-1 complex or plasma clot lysis time. Platelets may however also have functional effects on plasma fibrinolytic potential in the presence of high platelet counts, such as in platelet-rich plasma.

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Synergy between plasminogen activator inhibitor-1 and Snail in tumoral migration

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